科研成果详情

题名SARM1 deletion in parvalbumin neurons is associated with autism-like behaviors in mice
作者
发表日期2022-07-22
发表期刊CELL DEATH & DISEASE   影响因子和分区
语种英语
原始文献类型Article
其他关键词SPECTRUM DISORDER ; MOUSE MODEL ; NEUROINFLAMMATION ; REGULATOR ; DEFICITS ; NETWORK ; PROTEIN ; MEMORY
摘要Autism spectrum disorder (ASD), a group of neurodevelopmental disorder diseases, is characterized by social deficits, communication difficulties, and repetitive behaviors. Sterile alpha and TIR motif-containing 1 protein (SARM1) is known as an autism-associated protein and is enriched in brain tissue. Moreover, SARM1 knockdown mice exhibit autism-like behaviors. However, its specific mechanism in ASD pathogenesis remains unclear. Here we generated parvalbumin-positive interneurons (PVI)-specific conditional SARM1 knockout (SARM1(PV)-CKO) mice. SARM1(PV)-CKO male mice showed autism-like behaviors, such as mild social interaction deficits and repetitive behaviors. Moreover, we found that the expression level of parvalbumin was reduced in SARM1(PV)-CKO male mice, together with upregulated apoptosis-related proteins and more cleaved-caspase-3-positive PVIs, suggesting that knocking out SARM1 may cause a reduction in the number of PVIs due to apoptosis. Furthermore, the expression of c-fos was shown to increase in SARM1(PV)-CKO male mice, in combination with upregulation of excitatory postsynaptic proteins such as PSD-95 or neuroligin-1, indicating enhanced excitatory synaptic input in mutant mice. This notion was further supported by the partial rescue of autism-like behavior deficits by the administration of GABA receptor agonists in SARM1(PV)-CKO male mice. In conclusion, our findings suggest that SARM1 deficiency in PVIs may be involved in the pathogenesis of ASD.
资助项目National Natural Science Foundation of China [92049104, 31871042, 81971172]; Xinmiao Talents Program of Zhejiang Province, China [2021R413079]
出版者SPRINGERNATURE
出版地LONDON
ISSN2041-4889
卷号13期号:7页码:638
DOI10.1038/s41419-022-05083-2
页数11
WOS类目Cell Biology
WOS研究方向Cell Biology
WOS记录号WOS:000829054000001
收录类别SCIE ; PUBMED ; SCOPUS
URL查看原文
PubMed ID35869039
SCOPUSEID2-s2.0-85134616293
通讯作者地址[Wang, Wei]School of Mental Health,Wenzhou Medical University,Zhejiang,Wenzhou,325035,China ; [Huang, Zhihui]School of Mental Health,Wenzhou Medical University,Zhejiang,Wenzhou,325035,China
Scopus学科分类Immunology;Cellular and Molecular Neuroscience;Cell Biology;Cancer Research
TOP期刊TOP期刊
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被引频次:1[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符https://kms.wmu.edu.cn/handle/3ETUA0LF/154365
专题精神医学学院
基础医学院(机能实验教学中心)
第一临床医学院(信息与工程学院)、附属第一医院
附属第一医院
卓越中心_老年研究院
其他_附属康宁医院(温州市康宁医院)
通讯作者Wang, Wei; Huang, Zhihui
作者单位
1.School of Mental Health,Wenzhou Medical University,Zhejiang,Wenzhou,325035,China;
2.Tongde Hospital of Zhejiang Province,Zhejiang,Hangzhou,310012,China;
3.Department of Orthopedics (Spine Surgery),The First Affiliated Hospital of Wenzhou Medical University,Zhejiang,Wenzhou,325000,China;
4.Department of Child Psychiatry,Shaoxing Seventh People’s Hospital,Zhejiang,Shaoxing,312000,China;
5.School of Basic Medical Sciences,Wenzhou Medical University,Zhejiang,Wenzhou,325035,China;
6.Zhejiang Provincial Clinical Research Center for Mental Disorders,The Affiliated Wenzhou Kangning Hospital,Wenzhou Medical University,Zhejiang,Wenzhou,325000,China;
7.Institute of Aging,Key Laboratory of Alzheimer’s Disease of Zhejiang Province,Wenzhou Medical University,Zhejiang,Wenzhou,325035,China;
8.College of Pharmacy,Hangzhou Normal University,Zhejiang,Hangzhou,311121,China
第一作者单位精神医学学院
通讯作者单位精神医学学院
第一作者的第一单位精神医学学院
推荐引用方式
GB/T 7714
Xiang, Ludan,Wu, Qian,Sun, Huankun,et al. SARM1 deletion in parvalbumin neurons is associated with autism-like behaviors in mice[J]. CELL DEATH & DISEASE,2022,13(7):638.
APA Xiang, Ludan., Wu, Qian., Sun, Huankun., Miao, Xuemeng., Lv, Zhaoting., ... & Huang, Zhihui. (2022). SARM1 deletion in parvalbumin neurons is associated with autism-like behaviors in mice. CELL DEATH & DISEASE, 13(7), 638.
MLA Xiang, Ludan,et al."SARM1 deletion in parvalbumin neurons is associated with autism-like behaviors in mice".CELL DEATH & DISEASE 13.7(2022):638.

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